Columbia University Medical Center/The Cardiovascular Research Foundation, New York, New York 10022, USA.
JACC Cardiovasc Imaging. 2013 Jan;6(1):86-95. doi: 10.1016/j.jcmg.2012.08.010.
The authors sought to report the temporal stability of an untreated, nonculprit lesion phenotype in patients presenting with ST-segment elevation myocardial infarction (STEMI).
The temporal stability of the untreated, nonculprit lesion phenotype has been studied using intravascular ultrasound-virtual histology (IVUS) in patients with stable ischemic heart disease, but not in STEMI patients.
As part of a formal substudy of the HORIZONS-AMI (Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction) trial, baseline and 13-month follow-up IVUS was performed in 99 untreated nonculprit lesions in 63 STEMI patients. Lesions were classified as pathological intimal thickening (PIT), IVUS-derived thin-cap fibroatheroma (TCFA), thick-cap fibroatheroma (ThCFA), fibrotic plaque, or fibrocalcific plaque.
The frequency of TCFA increased from 41% at baseline to 54% at follow-up, whereas ThCFAs decreased from 41% to 34% and PIT decreased from 16% to 8%. Among the 41 lesions classified at baseline as TCFA, at follow-up, 32 (78%) were still classified as TCFA, whereas 9 (22%) were classified as ThCFAs or fibrotic plaques. An additional 21 lesions at follow-up were newly classified as TCFA, developing from either PIT or ThCFA. TCFA at baseline that evolved into non-TCFAs trended toward a more distal location than TCFA that did not change (p = 0.12). In lesions classified as TCFA, the minimum lumen area (MLA) decreased from 8.1 (interquartile range [IQR]: 7.4 to 8.8) mm(2) at baseline to 7.8 (IQR: 7.2 to 8.4) mm(2) at follow-up, p < 0.05; this was associated with an increase in percent necrotic core at the MLA site (14% [IQR: 12 to 16] to 19% [IQR: 17 to 22], p < 0.0001) and over the entire length of the lesion (14% [IQR: 12 to 16] to 18% [IQR: 17 to 20], p < 0.0001).
Untreated nonculprit lesions in STEMI patients frequently have TCFA morphology that does not change during 13-month follow-up and is accompanied by a decrease in MLA and an increase in necrotic core. (Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction [HORIZONS-AMI]; NCT00433966).
作者旨在报告 ST 段抬高型心肌梗死（STEMI）患者中未经治疗的非罪犯病变表型的时间稳定性。
在稳定性缺血性心脏病患者中，已经使用血管内超声-虚拟组织学（IVUS）研究了未经治疗的非罪犯病变表型的时间稳定性，但在 STEMI 患者中尚未进行研究。
作为 HORIZONS-AMI（急性心肌梗死血运重建与支架治疗的协调结果）试验的正式子研究的一部分，对 63 例 STEMI 患者的 99 个未经治疗的非罪犯病变进行了基线和 13 个月的 IVUS 随访。病变分为病理性内膜增厚（PIT）、基于 IVUS 的薄帽纤维粥样瘤（TCFA）、厚帽纤维粥样瘤（ThCFA）、纤维斑块或纤维钙化斑块。
TCFA 的频率从基线时的 41%增加到随访时的 54%，而 ThCFA 从 41%降至 34%，PIT 从 16%降至 8%。在基线时分类为 TCFA 的 41 个病变中，有 32 个（78%）在随访时仍被分类为 TCFA，而 9 个（22%）被分类为 ThCFA 或纤维斑块。在随访时，另外 21 个病变新分类为 TCFA，这些病变是由 PIT 或 ThCFA 发展而来的。从 PIT 或 ThCFA 演变而来的 TCFA 向更远端的位置发展的趋势大于未发生变化的 TCFA（p = 0.12）。在被分类为 TCFA 的病变中，最小管腔面积（MLA）从基线时的 8.1（四分位距 [IQR]：7.4 至 8.8）mm²降至随访时的 7.8（IQR：7.2 至 8.4）mm²，p < 0.05；这与 MLA 部位坏死核心百分比的增加有关（14%[IQR：12 至 16]至 19%[IQR：17 至 22]，p < 0.0001）和整个病变长度的增加（14%[IQR：12 至 16]至 18%[IQR：17 至 20]，p < 0.0001）。
STEMI 患者未经治疗的非罪犯病变常有 TCFA 形态，在 13 个月的随访中不会发生变化，并且伴随着 MLA 的减少和坏死核心的增加。（急性心肌梗死血运重建与支架治疗的协调结果 [HORIZONS-AMI]；NCT00433966）。
